Blood Flashcards

1
Q

What initiates the intrinsic pathway of coagulation?

A

The subendothelial damage

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2
Q

What initiates the extrinsic pathway of coagulation?

A

The contact of blood to traumatized tissue

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3
Q

What is the intrinsic pathway cascade?

A

Factor 12 activates 11, then 11 activities 9 which activates 10 in the presence of 8

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4
Q

What is the extrinsic pathway cascade?

A

Traumatized tissues releases factor 3 which activates factor 7 and both of them together activates factor 10

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5
Q

What is the common pathway?

A

It starts with factor 10 being activated from the intrinsic or extrinsic pathway then factor 10 activates pro-thrombin to thrombin (factor2) which accordingly activates fibrinogen to fibrin (factor1)

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6
Q

What is hemophilia?

A

Deficiency of factor 8 mainly. It is x-linked disease. It might be acquired as an autoimmune disease but mostly appears in children.

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7
Q

What is the coagulation/bleeding profile in hemophilia?

A

⬆️APTT
Normal PT
Normal bleeding time

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8
Q

What is VWD (Avon Willbrand Disease)?

A

Deficiency of VW factor which is a glycoprotein that helps is platelet adhesion and serves as plasma carrier for factor 8.
It is diagnosed by desmopressin test, that assess the VWF antigen and activity. And treated by Cryoprecipitate (1,8,13,VWF)

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9
Q

What is the coagulation/bleeding profile in VWD?

A

⬆️APTT
⬆️Bleeding time
Normal PT

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10
Q

What are the most common hypercoagulability diseases?

A

Factor 5 Leiden
Anti-Phospholipid disease
Anti-Thrombin 3 deficiency
Protein C and S deficiency

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11
Q

What is Factor 5 Leiden?

A

It is the most common genetic disease that causes DVT &PE

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12
Q

What is anti-phospholipid disease?

A

The most common cause of DVT in pregnant woman with positive family history. Prolonged APTT

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13
Q

What are the antibodies present in antiphospholipid disease?

A

Anticardiolipin
Lupus anticoagulant antibody

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14
Q

What is the treatment of Anti-Thrombin 3 deficiency?

A

Warfarin for life

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15
Q

What is protein C and S?

A

These are proteins formed in the liver as vitamin K dependent factors (1972).
Thrombomodulin with thrombin forms a complex which activates protein C to active protein C which accordingly -in presence of protein S- inhibits factor 5 and 8.

So their deficiency cause hyper coagulability

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16
Q

What are parental anticoagulants?

A

LMWH (clexan) & unfractionated heparin

17
Q

What are oral anticoagulants?

A

Warfarin (marivan)

18
Q

How heparin works?

A

LMWH: ⬇️Factor 10 and doesn’t need follow up (but long half life)

Unfractionated heparin: binds with antithrombin 3 forming a complex that ⬇️ factors 2,9,10,11

The APTT must be 2-3 folds of normal

19
Q

How does warfarin work?

A

It inhibits the vitamin K dependent factors 1972

Target PT is 2-3 folds of normal

20
Q

When and how to stop the action of heparin?

A

If LMWH: 12-24 hours before surgery
If Unfractionated heparin: 4-6 hours before surgery

The antidote is protamine sulfate

21
Q

What are the complications of heparin?

A

-Bleeding
-Heparin induced thrombocytopenia (HIT)
-Hyperkalemia (due to⬇️Aldosterone)
-Osteoporosis

22
Q

When and how to stop the action of warfarin?

A

-It should be stopped 3-5 days before a surgery.

-If we need immediate reversal, then IV Vitamin K with PCC
If not rapid reversal then oral vitamin K

-IV Vit K works in 4 hours so that why PCC (Prothrombin complex concentrate) must be given with if as it works in 1 hour

-Oral Vit K works in 24 hours

-If PCC is not available, fresh frozen plasma might be given as an alternative with Vit K but with close monitoring (risk of overload)

23
Q

How does the fibrinolytic system work?

A

The plasminogen is activated by the tissue plasminogen activator to plasminogen which dissolves fibrin threads

24
Q

What is tranexamic acid (kepron)?

A

It inhibits the plasminogen to decrease or control bleeding

25
Give examples of microcytic, macrocytic and normocytic anemias.
Microcytic: -Iron deficiency anemia Macrocytic: -Folic acid deficiency -Vitamin B12 deficiency Normocytic: -Hemorrhage or blood loss -Anemia of Chronic disease as CKD (⬇️erythropoietin deficiency) -Hemolytic anemia
26
What are the causes of vitamin B12 deficiency?
-Pernicious anemia (autoimmune disease attacking the parietal cells that produces intrinsic factor) -Gastrectomy -Ileal resection -Crohn’s disease
27
What are the MCV (mean corpuscular volume) in different types of anemias?
Micro <80 Macro >100 Normo 80-100
28
What are the expected serum ferritin levels and TIBC (total iron binding capacity) in Iron deficiency anemia/ chronic blood loss and Chronic illness anemia?
1-Iron deficiency anemia/chronic blood loss- S.ferritin is low and TIBC is high 2-Chronic illness anemia- S.ferritin is high and TIBC is low
29
What is sickle cell anemia?
It is a hereditary hemoglobinopathy (autosomal recessive) due to replacement of glutamate with valine that leads to: 1-Red cell distortion 2-Microvascular obstruction 3-Hemolytic anemia 4-Pigmented stones
30
When does sickle cell anemia manifest, what precipitates it and how is it diagnosed?
It manifests at 6 months, precipitated by dehydration, infection and hypoxia and diagnosed by HB electrophoresis and blood film.
31
What are the complications of Sickle cell anemia?
-Vaso-occlusive crisis: limbs (hands and foot syndrome), brain (stroke and retinopathy), lungs (chest syndrome), spleen (auto splenectomy) -Aplastic crisis: due to parvovirus infection -Sequestration crisis: in children, massive entrapment of Sickle cells in the spleen leading to splenic enlargement and hypovolemic shock
32
What is hereditary spherocytosis?
Is is common in Caucasian, in which the red cell membrane in abnormal and prone to destruction. This leads to: -Hemolysis -Hyperbilirubinemia (unconjugated) -Multiple small pigmented stones -Jaundice and splenomegaly Treated by: Splenectomy
33
What is cori cycle/ lactic acid cycle/ anerobic glycolysis?
It is the anaerobic convergence of glucose to pyruvate then lactic acid and it happens aerobically in erythrocytes as it doesn’t have mitochondria.